Genetically hypertensive rats are considered an important model of human essential hypertension. The focus of this study is the investigation of renal function in the hypertensive rats in relation to altered metabolism of prostaglandins by the kidney resulting from a deficiency of prostaglandin dehydrogenase. Renal vascular resistance is markedly increased in genetically hypertensive rats; this increase appears to be actively maintained as a response to increased perfusion pressure. Despite the reduced level of prostaglandin dehydrogenase, excretion of urinary prostaglandins by genetically hypertensive rats is not different from that of normotensive rats. In addition, the hyperresponsiveness of genetically hypertensive rat kidneys to infused prostaglandins does not appear to result from the altered catabolic capacity, since the degree of metabolism of infused prostaglandins is similar for hypertensive and normotensive rat kidneys. Two positive observations are the following. First, blood pressure of genetically hypertensive rats falls to normal levels during the 3-5 days before and 1-2 days after partuition, indicating that mechanisms extent within the hypertensive rat are capable of restoring normotension. Second, denervation of the kidneys of genetically hypertensive rats at 21 days of age delays the development of hypertension by about three weeks, approximately the time required for reinnervation to occur. This finding could indicate increased sympathetic nerve activity or increased renal sensitivity to sympathetic nerve activity, or both.